It has been estimated that up to 15,000 children born each year in the United States are affected by one or more symptoms of fetal alcohol syndrome (FAS). FAS includes central nervous system disturbances, characteristic facial malformations, other skeletal and soft tissue malformations, and prenatal and postnatal growth retardation. Growth retadation is one of the most prevalent features of FAS. A large number of tissues and processes that influence prenatal and postnatal growth are adversely affected by alcohol consumption during pregnancy, including endocrine systems that regulate growth. The overall goal of this project is to assess consequences of prenatal alcohol exposure on endocrine systems that regulate prenatal and postnatal growth using the mouse as an animal mode. Mice will be treated with alcohol beginning on day 5 of pregnancy and continuing until parturition. Alcohol will be administered in a liquid diet. Changes in food consumption due to alcohol will be controlled for by including both pair-fed controls and controls fed ad libitum in all experiments. To determine whether prenatal alcohol exposure affects circulating concentrations of hormones that regulate growth, the concentrations of placental lactogen, growth hormone, somatomedins and insulin in the maternal and fetal serum and in amniotic fluid will be determined in alcohol-treated and control mice at several times during pregnancy. In addition, concentrations of growth hormone, somatomedins and insulin will be measured in the offspring of alcohol-treated animals at different ages. To determine whether prenatal alcohol exposure affects the sensitivity of target tissues to growth regulating hormones, basal and hormone-stimulated hepatic glycogen synthesis, ornithine decarboxylase activity, somatomedin production, skeletal muscle amino acid uptake, and cartilage metabolism will be examined in alcohol-exposed and control fetal and postnatal mice.